The WNT (Wingless and INT-1) signal transduction cascade is mediated by Wnt proteins and is involved in cell survival and proliferation as well as cell fate and movement. [1, 2] In the absence of Wnt proteins the transcriptional regulator β-catenin is recruited into a destruction complex that contains Adenomatous Polyposis Coli (APC) and Axin (FIG. 1a). This event facilitates the phosphorylation of β-catenin by casein kinase 1 (CK1) and glycogen synthase kinase-3β (GSK-3) leading to ubiquitination and proteasomal degradation of β-catenin. Therefore, in the inactive state, cells maintain low levels of β-catenin. In the nucleus, target genes of the pathway are kept in a repressed state by interacting with T-cell factors (TCF) in association with co-repressors such as Groucho. The activation of signaling is facilitated by segregation of Wnt proteins which act on target cells by binding to the Frizzeld (Fz)/low density lipoprotein related receptor (LRP) complex at the cell surface (FIG. 1b). The formation of the receptor complex involves the binding of Dishevelled (Dsh) and Axin. This inhibits the formation of the destruction complex and allows accumulation of β-catenin in the cytosol and nucleus where it interacts with DNA-bound TCF to activate the transcription of target genes.